Journal of Pakistan Association of Dermatologists 2009; 19: 34-37.

Review Article
Diabetic’s skin; a storehouse of infections
Saifullah, Ghulam Mujtaba

Department of Dermatology, Nishtar Medical College & Hospital, Multan

Abstract Diabetes mellitus is a major endocrine cause of morbidity and mortality all over the world.
The incidence is increasing globally. Estimated number of patients with diabetes mellitus in
2030 is 366 million. In Pakistan, prevalence approaches 10% among adults and even greater
number with glucose intolerance. Patients with diabetes mellitus are prone to have cutaneous
infections and major underlying cause is hyperglycemia and ketoacidosis leading to immune
dysfunction. These infections can get complicated and even can prove fatal if not noticed
earlier or treated properly. It is important to recognize signs and symptoms of these and to
either treat them appropriately or refer the patient to a dermatologist or diabetologist. This
article is a brief review of clinical features, relative occurrence in diabetes mellitus, and
general management of several cutaneous infections which occur more commonly, with
greater severity; or with a greater risk for complications in patients with diabetes mellitus.

Key words
Diabetes mellitus, hyperglycemia, cutaneous infections

Introduction Pathogenesis

Diabetes mellitus (DM) is characterized by Much research has been undertaken on

state of relative or complete insulin deficiency,
leading to gross defects in glucose, fat and
protein metabolism. 1 It is a major endocrine
cause of morbidity and mortality all over the
world. The incidence is increasing globally.
Estimated number of patients with diabetes
mellitus in 2030 is 366 million.2 In Pakistan,
prevalence approaches 10% among adults and
even greater number with glucose intolerance.3
Recent studies show greater incidence of skin
infections in diabetic patients. Incidence
ranges from 20-50%,4 mostly in type 2
diabetes mellitus and often associated with
poor glycemic control.5 Infections constitute
the main bulk of cutaneous manifestations of
diabetes mellitus.6
Address for correspondence
Dr. Saifullah,
Department of Dermatology,
Nishtar Medical College & Hospital, Multan
Email: drsaif185@gmail.com
pathogenesis of the immune dysfunction in
diabetes mellitus. Studies show that leukocyte
chemotaxis, adherence and phagocytosis are
impaired, especially during hyperglycemia and
diabetic acidosis7and changes are even
reversible with lowering glucose level10.There
is also evidence that cutaneous T cell function
and response to antigen challenge are also
decreased in diabetes mellitus8. Diabetic
neuropathy and peripheral vascular
insufficiency favor the installation and
development of skin infection. In other words,
the diabetic's skin ends up being an organ
open to the most varied forms of affliction,
especially of infectious origin. It facilitates
complications and/or delays curing of
processes that are apparently benign and of
short duration.
Skin infections
Bacterial infections

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Journal of Pakistan Association of Dermatologists 2009; 19: 34-37.
Diabetics are at higher risk for contracting
certain bacterial infections including group A
and B streptococcal infections, necrotizing
fasciitis and malignant otitis externa.
a) Group B streptococcal infections
Group B streptococcus, a major cause of
morbidity in neonates and pregnant women, is
also a significant source of invasive bacterial
infections in non pregnant adults. Studies
show diabetes mellitus to be a risk factor in
these infections.9 Most common sites of
infections are skin, soft tissue and bone
(cellulitis, foot ulcers and decubitus ulcers). 9
Presence of diabetes in young adults increases
the risk of group B streptococcal infection 30
fold.3 Despite therapy, approximately 20% of
these cases are fatal. In pregnancy, maternal
diabetes mellitus (but perhaps not gestational
diabetes alone) increases the risk even more.
Group B streptococci remain susceptible to
penicillin G, ampicillin, and other
semisynthetic penicillins, although the MIC of
penicillin is frequently 4-fold to 8-fold higher
for group B streptococci than for group A
streptococci. Abscess drainage and
debridement of devitalized tissue are essential
when loculated fluid or necrosis is present 9
b) Group A streptococcal infections
In a prospective study, risk of skin and soft
tissue infections with group A streptococcus
was almost 4 fold greater in patients with
diabetes11. Soft infections were the most
common clinical presentation for all patients.
c) Staphylococcal infections
Although some old recommendations suggest
testing the patients with recurrent furunculous
or folliculitis for diabetes mellitus but recent
data do not permit estimation risk of
staphylococcal infections in diabetes mellitus.
Pyodermic infections such as impetigo,
folliculitis, carbuncles, furunculosis, ecthyma,
and erysipelas if present can be more severe
and widespread in diabetic patients. 4 Therapy
consists of adequate diabetic control and, if
necessary, adequate systemic antibiotic
therapy; deeper infections require intravenous
antibiotics.
d) Malignant otitis externa
Invasive malignant otitis externa is an
uncommon life-threatening infection of
external auditory canal with potential cranial
bone and intra cranial involvement.
Pseudomonas aeruginosa is usually implicated
and preceding aural irrigation with tap water
may play an etiologic role. This painful
infection, which occurs in older patients with
diabetes mellitus, is characterized by purulent
discharge, unilateral facial swelling, hearing
loss, and granulation tissue in the ear canal.
Approximately 70-94%of patients with
malignant otitis externa have underlying
diabetes7.Laboratory studies generally reveal
normal WBC count but raised ESR.CT and
MRI are essential for defining the extent of
bone and soft tissue involvement Treatment
consists of irrigation and drainage of the ear
canal, antibiotics, and sometimes debridement.
Diagnosis is often delayed and mortality rates
as high as 20-40% despite appropriate anti
biotic therapy.8
e) Necrotizing fasciitis
10-60% of all cases of necrotizing fasciitis
occur in patients with diabetes mellitus.12,13 It
is a life threatening bacterial infection of the
soft tissue with spread along facial planes. The
perenium, trunk, abdomen and upper
extremities are most commonly involved7.
Clinical presentation includes eryhtema,
swelling, induration, necrosis and possible
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Journal of Pakistan Association of Dermatologists 2009; 19: 34-37.
bullae formation. Degree of pain and toxicity
are out of proportion to the severity of the
findings. Although most cases result from
polymicrobial facultative gram negative bacilli
such as Escheracia coli and anaerobes such as
bacteroids, peptoptreptococcus and
clostridium species, approximately 10% cases
are monomicrobial often due to streptococcal
species. Treatment includes urgent surgical
debridmentand appropriate antibiotics.
Mortality rates of 40% have been reported.
Fungal and yeast infections
a) Candidal infections
Mucocutaneous Candida infections occur
more frequently among patients with diabetes
mellitus, especially those with poorly
controlled disease3. Candidal infection
(moniliasis) can be an early sign of
undiagnosed diabetes. Perlèche is a classic
sign of diabetes in children, and localized
candidal infection of the female genitalia
(vulvovaginitis) has a strong association with
diabetes. It is important to remember that in
men, Candida balanitis, and intertrigo
(axillary, inguinal web space), can be
presenting signs of diabetes. 4 Paronychia,
onychomycosis and glossitis are also common.
Treatment for candidal infections includes
topical and oral antifungals. Patients with
candidal paronychia should avoid wetting of
the nails and use drying agents.
b) Dermatophyte infections
Association of dermatophyte infection with
diabetes is controversial but recent data shows
a statistically significant relationship14.
.Common superficial infections are caused by
Trichophyton rubrum, T mentagrophytes, and
Epidermophyton floccosum. In diabetic
patients, onychomycosis or tinea pedis should
be monitored and treated, as it can be a port of
entry for infection. This is especially true for
patients with neurovascular complications and
intertrigo.
Signs of T. rubrum infection are noninflamed,
white, powdery scaling of skin creases on the
palms and soles, often with nail involvement.
T mentagrophytes-associated intertrigo or
interdigital infection presents as maceration
and superficial scaling with an active red
border. Treatment of choice is drying the local
area and applying one of the newer topical
imidazole antifungal agents.4
c) Rhinocerebral mucormycosis
Rhinocerebral mucormycosis (RCM) is caused
by zygomycetes (Mucor and Rhizipus species)
which often presents with headache, fever and
lethargy in addition to nasal congestion and
facial-ocular pain and swelling. Subsequent
findings include unilateral proptosis,
ophthalmoplegia and palate or nasocutaneous
necrosis.75-80% of all cases occur in patients
with diabetes mellitus, with diabetic
ketoacidosis as the most important risk
factor.3,15,16 Early diagnosis, aggressive surgical
debridment, high dose amphotericin B and
good control of blood sugar are the most
important factors to decrease the morbidity
and mortality from this fungal disease.
Mortality rates of RCM range from 15-34%.3
In addition to RCM, mucor species have also
been observed complicating skin ulcers on
legs and hands of diabetic patients.
Conclusion
Diabetic’s skin is more susceptible to skin
infections uncommon in non-diabetics. Many
of these infections require quick diagnosis and
immediate treatment if severe complications
or even fatal outcome is to be averted.
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Journal of Pakistan Association of Dermatologists 2009; 19: 34-37.

References 9 Farly MM. Group B streptococcal

disease in non-pregnant adults. Clin
Infec Dis 2001; 33: 556-61.
1 Bub JL, Olerud JE. Diabetes Mellitus:
10 Alba-Loureiro TC, Munhoz CD,
In Fitzpatrick TB, Freedberg IM, Eisen
Martins JO et al. Neutrophil function
AZ et al. (editors). Dermatology in
&metabolism in individuals with
General Medicine, Vol 2, 6th edn. New
diabetes mellitus. Brazilian J Med Biol
York: McGraw-Hill; 2003. p. 1651-55.
Res 2007; 40: 1037-44.
2 Wild S, Roglie G, Green A et al. Global
11 Sharkawy A, Low DE, Saginur R et al.
prevalence of diabetes. Diabetes Care
Severe group A streptococcal soft tissue
2004; 27: 1047-53.
infections in Ontario. Clin Inf Dis 2002;
3 Shera ASA, Jawad FA, Maqsood AA.
34: 454-60.
Prevalence of diabetes in Pakistan.
12 Oncul O, Erenoglu C, Top C et al.
Diabetes Res Clin Prac 2007; 76: 219-
Necrotizing fasciitis: A life-threatening
22.
clinical disorder in uncontrolled type 2
4 Hattemn SV, Boots MA, Thio HB. Skin
diabetic patients. Diabetes Res Clin
menifestations of diabetes. Cleveland
Pract 2008; 80: 218-23. Epub 2008 Jan
Clin J Med 2008; 75: 772-87.
10
5 Nigham PK, Pande S. Pattern of
13 Eke N. Fournier’s gangrene: A review
dermatoses in diabetics. Indian J
of 1726 cases. Br J Surg 2000; 87: 718.
Dermatol Venereol Leprol 2003; 69:
14 Aananthi C, Sarayu L. A study of
83-5.
chronic dermatophyte infection in a
6 Mahajan S, Koranne RV, Sharma SK.
rural hospital. Indian J Dermatol
Cutaneous manifestation of diabetes
Venereol Leprol 2005; 71: 129.
mellitus. Indian J Dermatol Venereol
15 Hsiao YC, Tsan KW, Wang TY.
Leprol 2003; 69: 105-8.
Rhinocerebral mucormycosis in
7 Olerud JE, editor. Ellenberg & Rifkin’s
diabetes. A case report. J Intern Med
Diabetes Mellitus, 6th edn. New York:
Taiwan 2002; 13: 160-4.
McGraw-Hill; 2003.
16 Hopkins MA, Treloa DM.
8 Joshi N, Caputo GM, Weitekamp MR,
Mucormycosis in diabetes. Am J
Karchmer AW. Infections in patients
Critical Care 1997; 6: 363-7.
with diabetes mellitus. N Engl J Med
1999: 341: 1906-99.

Erratum

In the case report ‘A case of acrogeria - a rare premature ageing syndrome’

published in the October-December 2008 issue of the Journal of Pakistan Association
of Dermatologists, page 235-237, the name of one of the authors was misprinted as
Noor Ilahi. The correct reference should be read as “Tahir Shehzad, Naveed Ilahi. A
case of acrogeria - a rare premature ageing syndrome. J Pak Assoc Dermatol 2008:
18(4): 235-237.”

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Journal of Pakistan Association of Dermatologists 2009; 19: 34-37.

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